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Analysis of gene network branching during optic cup morphogenesis in zebrafish (RNA-Seq)

ABSTRACT: We characterize transcriptomic landscape using RNA-seq in isolated NR and RPE populations in zebrafish.

ORGANISM(S): Danio rerio

PROVIDER: GSE150346 | GEO | 2021/05/06

REPOSITORIES: GEO

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Analysis of gene network branching during optic cup morphogenesis in zebrafish

Project description:We captured chromatin accessibility branching using ATAC-seq in isolated NR and RPE populations in zebrafish. We identify differentially active cis-regulatory modules and classify them as activating or repressing elements.

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Analysis of gene network branching during optic cup morphogenesis in zebrafish

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Analysis of gene network bifurcation during optic cup morphogenesis in zebrafish.

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Analysis of gene network branching during optic cup morphogenesis in zebrafish (RNA-Seq)

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Stretching of the retinal pigment epithelium contributes to zebrafish optic cup morphogenesis.

Project description:The vertebrate eye primordium consists of a pseudostratified neuroepithelium, the optic vesicle (OV), in which cells acquire neural retina or retinal pigment epithelium (RPE) fates. As these fates arise, the OV assumes a cup shape, influenced by mechanical forces generated within the neural retina. Whether the RPE passively adapts to retinal changes or actively contributes to OV morphogenesis remains unexplored. We generated a zebrafish Tg(E1-bhlhe40:GFP) line to track RPE morphogenesis and interrogate its participation in OV folding. We show that, in virtual absence of proliferation, RPE cells stretch and flatten, thereby matching the retinal curvature and promoting OV folding. Localized interference with the RPE cytoskeleton disrupts tissue stretching and OV folding. Thus, extreme RPE flattening and accelerated differentiation are efficient solutions adopted by fast-developing species to enable timely optic cup formation. This mechanism differs in amniotes, in which proliferation drives RPE expansion with a much-reduced need of cell flattening.

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Zebrafish mab21l2 mutants possess severe defects in optic cup morphogenesis, lens and cornea development.

Project description:BackgroundMutations in MAB21L2 result in severe ocular defects including microphthalmia, anophthalmia, coloboma, microcornea, and cataracts. The molecular and cellular underpinnings of these defects are unknown, as is the normal cellular function of MAB21L2. Zebrafish mab21l2 au10 mutants possess ocular defects resembling those in humans with MAB21L2 mutations, providing an excellent model to characterize mab21l2 functions during eye development.Resultsmab21l2 -/- mutants possessed a host of ocular defects including microphthalmia and colobomas as well as small, disorganized lenses and cornea dysgenesis. Decreased proliferation, increased cell death, and defects in marker gene expression were detected in the lens. Cell death in the optic stalk was elevated in mab21l2 -/- mutants and the basement membrane between the edges of the choroid fissure failed to break down. Neuronal differentiation in the retina was normal, however. mab21l2 -/- mutant corneas were disorganized, possessed an increased number of cells, some of which proliferated ectopically, and failed to differentiate the corneal stroma.Conclusionsmab21l2 function is required for morphogenesis and cell survival in the lens and optic cup, and basement membrane breakdown in the choroid fissure. mab21l2 function also regulates proliferation in the lens and cornea; in its absence, the lens is small and mispatterned, and corneal morphogenesis and patterning are also disrupted.

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Transcriptional analysis of forebrain plus optic cup from zebrafish embryos after BMP4 overexpression

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